ArticleFrontiers in pharmacology2020
Fitter Mitochondria Are Associated With Radioresistance in Human Head and Neck SQD9 Cancer Cells.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- The significance of mitochondrial DNA changes during the onset and progression of head and neck squamous cell carcinoma.Future oncology (London, England) · 2026Review
- Mitochondria-targeted strategies in cancer radiotherapy: from ROS regulation to immunogenic cell death.Frontiers in cell and developmental biology · 2026Review
- Multi-parametric functional optical spectroscopy to monitor the metabolic and vascular changes in small head and neck tumorsBiomedical optics express · 2025Article
- The Nuclear-Encoded Cytochrome c Oxidase Subunit COX4-1 Enhances Hypoxia Tolerance in Glioblastoma Cells.Journal of oncology research and therapy · 2025Article
- Mitochondrial involvement in PC: improving therapeutic strategies.Frontiers in pharmacology · 2025Review
- Subclinical dose irradiation triggers human breast cancer migration via mitochondrial reactive oxygen species.Cancer & metabolism · 2024Article
- α-Ketoglutarate supplementation and NAD+ modulation enhance metabolic rewiring and radiosensitization in SLC25A1 inhibited cancer cells.Cell death discovery · 2024Article
- SHF confers radioresistance in colorectal cancer by the regulation of mitochondrial DNA copy number.Clinical and experimental medicine · 2023Article
- Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023Review
- Unraveling the Peculiar Features of Mitochondrial Metabolism and Dynamics in Prostate Cancer.Cancers · 2023Review
- Human papillomavirus-associated head and neck squamous cell carcinoma cells rely on glycolysis and display reduced oxidative phosphorylation.Frontiers in oncology · 2023Article
- Review
- Targeting Mitochondrial Metabolism to Reverse Radioresistance: An Alternative to Glucose Metabolism.Antioxidants (Basel, Switzerland) · 2022Review
- Mitochondrial Protein Cox7b Is a Metabolic Sensor Driving Brain-Specific Metastasis of Human Breast Cancer Cells.Cancers · 2022Article
- Biological Mechanisms to Reduce Radioresistance and Increase the Efficacy of Radiotherapy: State of the Art.International journal of molecular sciences · 2022Review
- Olaparib Is a Mitochondrial Complex I Inhibitor That Kills Temozolomide-Resistant Human Glioblastoma Cells.International journal of molecular sciences · 2021Article
- Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts.International journal of molecular sciences · 2021Review
- Targeting cancer-cell mitochondria and metabolism to improve radiotherapy response.Translational oncology · 2021Review
- Biological Adaptations of Tumor Cells to Radiation Therapy.Frontiers in oncology · 2021Review
- Radioresistance of Human Cancers: Clinical Implications of Genetic Expression Signatures.Frontiers in oncology · 2021Article
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The clinical management of head and neck squamous cell carcinoma (HNSCC) commonly involves chemoradiotherapy, but recurrences often occur that are associated with radioresistance. Using human SQD9 laryngeal squamous cell carcinoma cancer cells as a model, we aimed to identify metabolic changes associated with acquired radioresistance. In a top-down approach, matched radiosensitive and radioresistant SQD9 cells were generated and metabolically compared, focusing on glycolysis, oxidative phosphorylation (OXPHOS) and ROS production. The cell cycle, clonogenicity, tumor growth in mice and DNA damage-repair were assessed. Mitochondrial DNA (mtDNA) was sequenced. In a bottom-up approach, matched glycolytic and oxidative SQD9 cells were generated using FACS-sorting, and tested for their radiosensitivity/radioresistance. We found that acquired radioresistance is associated with a shift from a glycolytic to a more oxidative metabolism in SQD9 cells. The opposite was also true, as the most oxidative fraction isolated from SQD9 wild-type cells was also more radioresistant than the most glycolytic fraction. However, neither reduced hexokinase expression nor OXPHOS were directly responsible for the radioresistant phenotype. Radiosensitive and radioresistant cells had similar proliferation rates and were equally efficient for ATP production. They were equally sensitive to redox stress and had similar DNA damage repair, but radioresistant cells had an increased number of mitochondria and a higher mtDNA content. Thus, an oxidative switch is associated with but is not responsible for acquired radioresistance in human SQD9 cells. In radioresistant cells, more abundant and fitter mitochondria could help to preserve mitochondrial functions upon irradiation.
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